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In writing the names of the medicines is subject to all rules of spelling words of foreign origin as the basis for their creation was the Latin language sucralfate 1000mg without prescription gastritis y sus sintomas. Paronyms are the words sound quite similar in composition and sound but different in meaning order sucralfate 1000mg otc chronic gastritis low stomach acid. There are paronyms in many names sucralfate 1000 mg on line gastritis in spanish, including names that do not even belong to the same pharmacological group order sucralfate 1000mg overnight delivery gastritis flare up symptoms. Is not possible to avoid this phenomenon but we must be very careful with Paronyms. The use of paronyms which may be dangerous for patients may lead to dangerous consequences to human life. In forming trade names of medicines it‘s necessary to consider some general principles: possible brevity, euphony, no negative associations, originality, spelling and sound. I will consider what you need to study at American universities and to work in the specialty pharmacist, the pharmacy technologist, and many others. I will conduct a comparative description of the University in our city and University in the U. We consider the average annual salary of Americans who work in the pharmaceutical industry, and will draw appropriate conclusions. Moreover, show that pharmacists can earn enough money if you possess a profession on the level. And that our profession is not limited to the sale of tissues in the chemistry shop. From this we can see why this profession is such a high demand in the United States. And we should follow the example of our colleagues and gain experience from each other. Intensive development of phraseology in recent decades has raised a variety of questions. On the one hand, the description of phraseological material of different languages focusing on their specific features is the task of phraseological units, on the other hand, comparative study of phraseological systems become very important. The comparative aspect of system studying phraseology represents a great interest for the development of the general theory of phraseology, and for studing common and distinctive features of the investigated languages. The purpose of the study is to conduct a comparative analysis of Russian and Arabic idioms and identify their common and differential characteristics. In the research article were used next methods: etymological method when restoring original image internal forms of phraseological units; contrastive method when comparing Russian and Arabic idioms. Phraseological units are the most difficult for translating units; therefore, the translation of such units is the result of a careful analysis of the various components of the content structure of idioms. When translated an idiom we should convey its meaning and reflect its figurativeness, finding a similar expression in Russian and not losing the stylistic idiom function. If there is not the identical image in Russian translator is forced to finding approximate compliance. The Phraseological translation involves using stable units of varying degrees of proximity between the unit of the foreign language and the translated unit in the text. The most difficult translation from one language to another is part of phraseological units, which are based on historical events; reflect some custom of Russian people or Arabs or use specific words. Lingvocultural researches provide the opportunity of implementation of the cognitive approach to comparative studying of phraseological units in order to identify their cultural specificity. It was found that in Russian phraseological units are dominated proverbs and sayings of the following type: statement, opposition, contraposition, metaphor and comparison, while in Arabic phraseological units‘ contraposition almost is not using. Actuality of the subject: one important terminological issue that today require solutions that use in scientific and educational literature in parallel to the two Latin names of the chemical element Arsenic, which leads to the operation of the different names of the same compounds, especially of the names of acids. Purpose: to analyze a certain volume of literature on the subject, to establish what the names of arsenic are we can find and how often, to infer what names are appropriate and properly applied in the academic literature. The chemical element Arsenic has been known and widely used already in ancient times. The Russian name is believed to have derived from "mouse" and "poison", because the use of drugs arsenic is associated with the extermination of mice and rats. Lavoisier had provided the arsenic metal and gave the element the name "Arsenicum". The research question, which we put before us is appropriate to begin with the editions of the alchemists, their works and articles. Our first source for treatment information has been scientifically-popular edition. From this article shows that the author uses the name Arsenic - arsenicum that is, the suffix -іс-. Searching for the right information we have not passed a security source - Materia Medica- scientific literature which takes ambiguous position to use the names of arsenic, indicating that the name is Arsenicum and Arsenum. Also ambiguous approach in the British Pharmacopoeia, where we found the name Anseni Trioxudum, putting the name of a chemical element with the compound in the nominative case, we get - Ansenum. Conclusion: we have been processed 16 educational, scientific publications and sources of Internet resources. After collecting the required amount of material, we noticed that both names are used arsenic - Arsenum, i n and Arsenicum, i n, as two names acids: acidum arsenicicum - acidum arsenicum and acidum arsenicosum - acidum arsenosum. In our opinion, avoiding dualism, is better to use the name element Arsenicum, and n and all derivative form it from its base. The appearance of new words or new meanings of old words means that, the world around us has changed. Either there something new has appeared, or something that has been existing has become so important, that the language, in fact, people who speak this language, create a name for them Aim. Consider and analyze some loan words which have appeared in Russian language in recent years. The research materials are the words of foreign origin, which have been partially or completely mastered by Russian language. It is not only the perception of words from other languages, but their creative development on all levels of language system, formal and semantic transformation according to the original features of Russian language and a high degree of its development. Foreign-language words were subjected to various kinds of changes (phonetic, morphological, semantic), submitting to the laws of development of the Russian language, its functional-stylistic norms. Correspondingly, it is accepted to allocate following stages of adoption of loan words: phonetic, graphical, grammatical and semantic. The process of mastering of words and expressions in Russian language causes us great interest, since at the current stage from long-term it has turned into one, which is happening right in our eyes. There is already a word with the same meaning, for example, a управляющий or colloquial управленец. However, the word менеджер (manager) is absolutely unique, and there is no substitute for it. Thus, contemporary texts, the names of professions, shops, cafes, restaurants, firms and etc. Will all these words included into Russian language or not, time will tell, and at this stage we can make only assumptions. There are many terms in Latin language, which name persons, who are engaged in education and tuition. The initial meanings of this word were the ruler, the boss, the manager and the supervisor. This word is related with the words magnus - large, magis – more, which have root mag.

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Treatment with methotrexate order sucralfate 1000mg gastritis diet dairy, mito- xantrone and mitomycin was followed by tamoxifen discount sucralfate 1000 mg without a prescription gastritis diet , medroxyprogesterone acetate or medroxyprogesterone acetate and radiation therapy sucralfate 1000mg amex gastritis diet zen. Acute myeloid leukaemia (one case of acute monoblastic leukaemia proven 1000mg sucralfate gastritis que es, one of acute promyelocytic leukaemia and one of acute undifferentiated leukaemia) occurred 12–30 months after the start of treatment with the mitoxantrone-containing regimen. The patient had been treated with high doses of corticosteroids during exacerbation of the multiple sclerosis. Five years before the diagnosis of acute promyelocytic leukaemia, the patient had received an intravenous dose of mitoxantrone (10 mg/m2) once a month for five months (total dose, 87. The patient was reported to have no history of exposure to known leukaemogenic risk factors or a personal or family history of malignancy. Partridge and Lowdell (1999) reported the development of myelodysplastic syndrome in a 62-year-old woman treated for advanced breast cancer with five courses of mitoxantrone (7 mg/m2), methotrexate and mitomycin. In addition, she had received radiotherapy to the breast and axilla and tamoxifen. The planned doses for the intravenous regimen that included mitomycin (n = 30) were: mitoxantrone, 8 mg/m2 every three weeks (total dose, 64 mg); mito- mycin, 8 mg/m2 every six weeks (total dose, 32 mg) and methothrexate, 30 mg/m2 every three weeks (total dose, 240 mg). The planned doses for the intravenous regimen that did not include mitomycin (n = 29) were: mitoxantrone, 12 mg/m2 every three weeks (total dose, 96 mg) and methothrexate, 35 mg/m2 every three weeks (total dose, 280 mg). During follow-up for a median of 72 months, two cases of acute myeloid leukaemia (one of acute myelomonocytic leukaemia and one of acute myeloblastic leukaemia) and one case of myelodysplastic syndrome occurred. All three patients had received treatment without mitomycin in combination with tamoxifen (three cases), radiotherapy (one case) or other cytostatic drugs (one case). The interval between treatment and diagnosis was 17 and 18 months for the cases of acute myeloid leukaemia and 36 months for the case of myelodysplastic syndrome. The frequency of acute myeloid leukaemia and myelodysplastic syndrome was 3/59 (5%) in the two treatment groups combined and 3/29 in the group given treatment without mitomycin, who had received a higher dose of mitoxantrone and a slightly higher dose of methotrexate than the group treated with mitomycin. The dose of mitoxantrone associated with leukaemia was higher than that usually given in the treatment of advanced breast cancer. These were not considered further because the follow-up was rarely longer than one year and the patients would previously have been treated with leukaemogenic agents and/or radiation. Studies of Cancer in Experimental Animals No data were available to the Working Group. There are no published data on the bio- availability of orally administered mitoxantrone in humans, but a number of studies have reported the pharmacokinetics of mitoxantrone given as an intravenous infusion over 3–60 min at doses of 1–80 mg/m2. All showed an initial rapid phase representing distri- bution of the drug into blood cells, with a half-time of about 5 min (range, 2–16 min) and a long terminal half-time of about 30 h (range, 19–72 h) (Savaraj et al. Many early studies reported much shorter terminal half-times, but suitably sensitive assays may not have been used or adequate numbers of late samples collected. Tri-exponential elimination has been reported, the second distribution phase having a half-time of about 1 h (Alberts et al. The extent of the distribution into blood cells is illustrated by the observation that at the end of a 1-h infusion, the concentrations of mito- xantrone in leukocytes were 10 times higher than those in plasma (Sundman-Engberg et al. The typical peak plasma concentration after a 30–60-min infusion of 12 mg/m2 was about 500 ng/mL (Smyth et al. The rapid disappearance from plasma results in a total plasma clearance rate of about 500 mL/min, while the large volume of distribution of 500–4000 L/m2 indicates tissue sequestration of the drug (Savaraj et al. Studies of patients given mitoxantrone at doses up to 80 mg/m2 (standard dose, 12 mg/m2) suggest that the kinetics is linear up to this dose (Alberts et al. Studies of the urinary excretion of mitoxantrone concur that little of the admin- istered dose is cleared renally. In one study, urinary recovery of radiolabel after intravenous administration of [14C]mito- xantrone accounted for 6. The elimination half-time of mitoxantrone in two patients with impaired liver function was 63 h, whereas that in patients with normal liver function was 23 h (Smyth et al. Faecal recovery of radiolabel after a single 12 mg/m2 dose was 18% (range, 14–25%) over five days (Alberts et al. These results suggest that the liver is important in the elimination of mito- xantrone and that patients with impaired liver function or an abnormal fluid compart- ment may be at increased risk for toxic effects. The sequestration of mitoxantrone by body tissues results in retention of the drug for long periods. The characteristic blue–green colour of mitoxantrone has been observed on the surface of the peritoneum more than one month after intraperitoneal administration, and the concentrations in peritoneal tissue 6–22 weeks after intra- peritoneal dosing ranged from < 0. Mito- xantrone was readily detectable in post-mortem tissue samples from all 11 patients who had received mitoxantrone intravenously between 10 and 272 days before death. The highest concentrations were found in the thyroid, liver and heart and the lowest in brain tissue (Stewart et al. In one patient given [14C]mitoxantrone intra- venously, who died 35 days after the dose, as much as 15% of the administered dose could be accounted for in the liver, bone marrow, lungs, spleen, kidney and thyroid glands (Alberts et al. In one study, the fraction of unbound drug in plasma at the end of a 30-min infusion was only 3. Because of its limited urinary excretion, little information is available on the meta- bolism of mitoxantrone. Two inactive metabolites were identified in urine as the mono- and dicarboxylic acid derivatives resulting from oxidation of the terminal hydroxy groups of the side-chains (Figure 1) (Chiccarelli et al. The concentrations of mitoxantrone in urine were not altered by pre-incubation with a β-glucuronidase or sulfatase, suggesting that the drug is not excreted renally as either the glucuronide or sulfate conjugate (Smyth et al. This metabolite has been identified in the urine of patients given mitoxantrone (Blanz et al. After two further courses of 6 mg/m2 mitoxantrone, her breast milk contained 120 ng/mL mito- xantrone 3–4 h after dosing and 18 ng/mL by five days, and the concentration remained at this level for 28 days. This finding indicates that the drug is slowly released from a deep tissue compartment (Azuno et al. The drug was not developed for oral use, and in a review mito- xantrone was described as being poorly absorbed when administered orally [species not mentioned] (Batra et al. In rats, dogs and monkeys, the disappearance of intravenously administered [14C]- mitoxantrone from plasma was rapid, followed by a slow terminal elimination phase (James et al. Extensive tissue binding was indicated, with 50, 25 and 30% of the dose still retained 10 days after intravenous administration in rats, dogs and monkeys, respectively. In beagle dogs, tri- exponential elimination from plasma was reported, with a very rapid initial distribution phase with a half-time of 6. Extensive tissue retention was again reported, the higher concentrations 24 h after dosing being found in the liver, kidney and spleen. Two metabolites were detected, accounting for 30% of the radiolabel in plasma and 50% in urine, but were not identified (Lu et al. A rapid distribution and a slow elimination phase were also observed in mice, with retention in body tissues, particularly liver and kidney (Rentsch et al. A naphthoquinoxaline metabolite of mitoxantrone has been reported in rats and pigs, resulting from the oxidation of the phenylenediamine substructure (Blanz et al. In general, mitoxantrone is believed to be active in mammalian cells in vitro in the absence of exogenous metabolic activation; however, inhibition of cyto- chrome P450 mixed-function oxidase by metyrapone in HepG2 hepatoxic cells and rat hepatocytes blocked the cytotoxic activity of mitoxantrone, suggesting that conversion to reactive species might be important (Duthie & Grant, 1989; Mewes et al. Leukopenia is the main dose-limiting effect, the lowest leukocyte counts typically being found 10–14 days after a single dose, with recovery by day 21. In a large European trial, seven of 264 patients experienced cardiac abnormalities (3%). Risk factors that may be predictive of the cardiotoxicity of this drug are previous anthracycline therapy, mediastinal radiotherapy and a history of cardiovascular disease (Crossley, 1983). The number of cardiotoxic events increases with cumulative doses of mitoxantrone > 120 mg/m2 in patients who have previously been treated with anthra- cyclines, and > 160 mg/m2 in patients who were not previously treated.

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As had been the case in the production of sera after 1895 quality 1000mg sucralfate gastritis diet virus, biological assays played a critical role in measuring the potency of every single batch of the processed material proven sucralfate 1000 mg gastritis diet soy sauce. The characterization of each batch with a reference number of “male” or “female” biological units was the frst and mandatory step in the defnition of the pharmacological dosages to be employed by doctors discount sucralfate 1000mg amex gastritis causas. As a consequence sucralfate 1000 mg gastritis treatment and diet, clinicians’ prescription practices relied on the same sort of bioassays as those of engineers. Legally defned professional responsibility of the pharmacist as drug manufacturer – biological or not – made the pharmacist liable if the composition of the products did not correspond to claims and if use under normal dosage and circumstances led to injuries. Standardized preparations were thought to be better and more reliable drugs, echoing the doctors’ quest for a more scientifc medicine. More precisely, Wertbestimmung as practiced in the testing laboratory did not aim only at the measurement of biological and – putative – clinical effects. Quantifying the concentration of active substance in a given batch was central to the surveillance and control of production. Testing was implemented at the end of the production process, and at the beginning as well, as routine control of the raw materials. As from the late 1920s, preparation of the female hormone started with the treatment 49 Wimmer, op. Schering collected large quantities of urine, frst from pregnant women and later from pregnant mares. The content of the incoming cans was regularly tested in Junkmann’s laboratory to verify that it was worth processing. When production shifted to the use of horses, this was also a way of controlling the work done by the farmers benefting from a supply contract. Another industrial function of the biological assay was to compare the effects of changes in the preparation process (modifying the nature of solvents, changing concentrations, or varying temperature and pressure), which were indispensable to transform new procedures envisioned by in-house scientists and engineers into full-fedged manufacturing practices. Biological assays of batches produced under different conditions thus became part of the industrial search for increased productivity. The third level of regulatory activities stems from Schering’s discussions with a limited number of trusted physicians who on a regular basis contributed clinical reports on the observations they had made with the frm’s sex hormones. This was the case, for instance, with the prescription of estrogens to reduce the sufferings of the menopausal transition, a practice many gynecologists contested. Based on these industrially defned guidelines, Schering’s regulation of prescription combined a palette of initiatives that included package design, trademark choice, the writing of package inserts, the dissemination of leafets and brochures providing examples of successful treatments, as well as standards of use. In the 1930s, these discussions, at the boundary between research, clinical standardization, and promotion diversifed into an authentic system of “scientifc marketing. Besides the organization of small conferences with “opinion leaders” in various medical specialties interested in a given type of products that enlarged the circle of “core” collaborators, a critical change was also the decision to launch Medizinische Miteilungen, a publication mimicking academic journals but juxtaposing direct advertisement and research reports originating either in Schering’s laboratory or in the collaborating clinical services, all of this supplemented with articles on the frm’s products directly reprinted from the medical press. Judging from the resonance obtained in the medical press by some of the therapeutic regimens promoted by Schering – such as the combined administration of estrogens and progesterone to create an artifcial reproductive cycle and cure amenorrhea – it was far from negligible. Conclusion Contemporary France has the reputation of being a country that invented a unique alliance between private industrial frms and state administration. Labeled as “Colbertism,” this 51 J-P Gaudillière, “Genesis and Development of a Biomedical Object: Styles of Thought, Styles of Work and the History of the Sex Steroids”, Studies in History and Philosophy of the Biological and the Biomedical Sciences, 2003, 34 : 32-55. During the twentieth century, it supposedly led French high-ranking civil servants trained in the country’s major engineering schools such as the École des Mines or the École Polytechnique, which staffed the state’s technical bodies, to work in close connection with private capitalistic entrepreneurs in order to further industrial investments, scale up production, protect the national markets, and rescue, if needed, threatened strategic enterprises or banks. Echoing previous work showing the slow transformation of the French pharmaceutical frms into large corporations, this paper actually documents a different pattern, linking a scattered economic landscape with diversifed forms of industrialization and innovation. Two features of the twentieth-century regulatory landscape are hence worth emphasizing. Strong professional regulation resulted in the absence (until the 1941 establishment of the visa system) of any form of pre-marketing evaluation organized under the authority of the state. As many observers of French medicine have noticed, the central state health administration was anemic and without much power. The trajectories of plant extracts and organ therapy discussed here confrm what has been documented when comparing the regulation of sera in France and Germany. True, biological therapies, due to their novelty in the pharmacopoeia, their variability, and their potency, were granted a special status. Even when sera or hormones were considered, however, this special status was limited to a system of preliminary authorization – with or without inspection – of the production facility. Rather than being a means for drug surveillance, this control refected the current understanding of professional autonomy. When acting as experts, physicians and pharmacists were left alone to decide what drugs were worth producing and prescribing, whereas when acting as producers, their legal responsibility was the same as that of any industrialist, i. A second, less expected dimension of this professional regulation focuses on the type of knowledge associated with the critical function granted to the pharmacopoeia. The assumed consequence is then that a chemical paradigm centered on the purifcation, the structural description, and – when possible – the synthesis of therapeutic substances dominated the culture in parallel with the pharmacological model of the relationship between doses and effects mentioned in the introduction to this volume. In contrast to this assumed connection, the cases analyzed here suggest that until late in the twentieth century, chemical entities barely played a role in the pharmacists’ world of preparation. Up to the 1920s, the receipts of the Codex did not favor making pure, molecular entities, but rather making stable, reliable compositions of medical matters, a majority of which originated in living (mostly plant) bodies. A pharmacists’ culture of preparation that owed little to the model of purifcation and synthesis dominated the early industrialization of drugs. This form of innovation placed value on the art of combining or the art of presenting known – and often complex – substances. As shown by the case of Dausse, such industrialization mobilized chemical tools as a means for concentration, control, and standardization, as well as marginally as a source of isolated substances. Complexes seemed especially valuable and important to preserve when plant extracts came under consideration. The industrialization of plant and organ extracts therefore relied on mechanics on the one hand and physiology on the other. The model of professional regulation advanced in our introductory chapter should therefore be amended to take into account this diversity of know-how, beyond the mere mobilization of pharmacological modeling. As illustrated here, biological testing systems were not just important elements in the industrial practice of standardization and quality control. In parallel, academic pharmacists used them to perform physiological functions and make them manifest, meaning that they became tools to explore and signal the synergies and complexities that remained central to the culture of preparations. If there is a caricature of German history to parallel the image of the French industrial state, it is the idea of a rapidly growing chemical industry that colonized the entire pharmaceutical sector after the 1890s. One major interest of the history of plant extracts is to show the importance of these practices, which made a subset among German frms comparable to their French counterparts living off of the exploitation of specialties registered in the pharmacopoeia. The history of Madaus thus reveals a culture of preparation that shares many aspects with the practices at Dausse, including the organization of plant collection and breeding, mechanical innovations, a deep interest in physiological tools, and research. The social and intellectual landscape within which the frm blossomed was not the French professional order, but a rare combination of industry and alternative medicine. Madaus’s holistic approach of the living, which nurtured a system of correspondences among plants, animals, and human beings, than the integration of alternative medical practices – homeopathy, as well as the use of plants and organ extracts – into the industrial regulatory order and its values of productivity, standardization, and homogeneity, all of which were taken as synonymous of quality and effectiveness. The consequences were not only the prominent role attributed to mechanics and processing, but the mobilization of pharmacology and chemistry 63 Jean-Paul Gaudillière for quality control. As a company looking for a more scientifc form of popular and biological medicine, Madaus paradoxically engaged in the development of as many standards and assays as more molecularly oriented frms like Schering or Hoechst. The tensions brought about by this transformation of therapeutic agents previously associated with forms of medical practices stressing the individual and constitutional nature of disease into mass-produced and prescription- ready pills are easy to perceive, but remain to be analyzed. Similarly, comparison between Madaus and Schering highlights the commonalities of the industrial regulation of drugs. Both frms developed in-house research facilities focusing on physiology, both focused on biological assays as privileged tools of intervention, both invented relations with physicians and local practitioners that linked science and marketing.

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Mechanism of action: Stimulates receptors in androgen-responsive organs sucralfate 1000mg generic gastritis diet , thereby promoting growth and development of male sex organs generic sucralfate 1000 mg with amex gastritis pictures. Drug should be administered only by a physician who is aware of possible adverse effects of drug on bone maturation order sucralfate 1000mg without prescription gastritis tylenol. Contraindications: Hypersensitivity to testosterones generic sucralfate 1000mg with visa gastritis english, males with carcinoma of the breast, known or suspected carcinoma of the prostate, serious cardiac, renal, or hepatic decompensation; women who are or may become pregnant. Warnings/precautions: Prolonged use of androgens has been associated with peliosis hepatitis, cholestatic jaundice, hepatic neoplasms. Advice to patient • Notify physician for persistent erections in males, excessive facial hair, menstrual irregularities in women. Adverse reactions • Common: pruritis, edema, acne, gynecomastia, priapism, breast tenderness. Parameters to monitor • Intake of fluids and urinary and other fluid output to minimize renal toxicity. Editorial comments: Physicians who prescribe androgens including progesterone for nonapproved indications may be sub- ject to criminal prosecution. Antiemetic: Raises threshold stimulation of chemoreceptor trigger zone in medulla. Warnings/precautions • Use with caution in patients with hypertension, kidney disease. Advice to patient • Do not drive or operate machinery for several hours after taking this drug. Adverse reactions • Common: restlessness, drowsiness, fatigue, dizziness, diarrhea. Clinically important drug interactions • Drugs that increase effects/toxicity of metoclopramide: nar- cotic analgesics, phenothiazines, haloperidol. Editorial comments: In the majority of patients >65 years, treat- ment with metoclopramide should generally be avoided. Metolazone Brand names: Mykrox (rapid-release tablet), Zaroxolyn (slow- release tablet). Mechanism of action: Inhibits sodium reabsorption at critical dilution site of renal tubule. Other thiazide diuretics are considered compatible by American Academy of Pediatrics. Contraindications: Anuria, hepatic coma or precoma, hypersen- sitivity to metolazone. Editorial comments • Zaroxolyn must not be interchanged with other metolazone formulations as these differ greatly in bioavailability and thus are not bioequivalent. Mechanism of action: Competitive blocker of β-adrenergic receptors in heart and blood vessels. If necessary to dis- continue, taper as follows: Reduce dose and reassess after 1–2 weeks. Advice to patient • Avoid driving and other activities requiring mental alertness or that are potentially dangerous until response to drug is known. Clinically important drug interactions • Drugs that increase effects/toxicity of β blockers: reserpine, bretylium, calcium channel blockers. If hypotension occurs despite correction of bradycardia, adminis- ter vasopressor (norephinephrine, dopamine or dobutamine). Stop therapy and administer large doses of β-adrenergic bronchodilator, eg, albuterol, terbutaline, or aminophylline. Some advocate discontinuing the drug 48 hours before surgery; others recommend withdrawal for a considerably longer time. These are drugs of first choice for chronic stable angina, used in conjunction with nitroglycerin. Also, Treponema pallidum, oral spirochetes, Campylobacter fetus, Gardnerella vaginalis, Helicobacter pylori. Adjustment of dosage • Kidney disease: Creatinine clearance <10 mL/min: reduce dose by 50%. Safety and efficacy in children have not been established except in treatment of amebiasis. Considered contraindicated in the first trimester of pregnancy when used for trichomoniasis. Advice to patient • Avoid driving and other activities requiring mental alertness or that are potentially dangerous until response to drug is known. Adverse reactions • Common: headache, abdominal pain, anorexia, dizziness, vomiting. Clinically important drug interactions • Drugs that decrease effects/toxicity of metronidazole: barbitu- rates, phenytoin. Doses of 20 mg/kg/d for 3 months have been shown to prevent recurrence of Crohn’s disease following ileal resection. Mechanism of action: Suppresses automaticity and shortens effective refractory period in His-Purkinje conducting system. Onset of Arrhythmic Action Peak Effect Duration 30 min–2 h 2–3 h 8–12 h Food: Take with food or antacid. Advice to patient • Avoid driving and other activities requiring mental alertness or that are potentially dangerous until response to drug is known. Clinically important drug interactions • Drugs that increase effects/toxicity of mexiletine: cimetidine, other antiarrhythmic drugs, metoclopramide. If pulse rate falls to less than 50 beats/min or becomes irregular reduce or discontinue mexiletine. Susceptible organisms in vivo: Streptococcus pneumoniae, beta- hemolytic streptococci, Enterococcus faecalis, Escherichia coli, Hemophilus influenzae, Klebsiella sp, Neisseria gonorrhoeae, Proteus mirabilis, Salmonella sp, Shigella sp, Morganella mor- ganii, Proteus vulgaris, Providencia rettgeri, Providencia stuartii, Enterobacter sp, Citrobacter sp, Pseudomonas aerugi- nosa, Serratia sp, Acinetobacter sp, Clostridium sp, Peptococcus sp, Peptostreptococcus sp, Bacteroides sp, Fusobacterium sp, Eubacterium sp, Veillonella sp. Editorial comments • Mezlocillin is used to treat aerobic gram-negative infections. Mechanism of action: Thickens cell wall, thereby altering per- meability of fungal cell membrane. Susceptible organisms in vitro: Coccidioides immitis, Candida albicans, Cryptococcus neoformans, Histoplasma, Paracoccid- ioides, Brasiliensis. Clinically important drug interactions • Miconazole increases effects/toxicity of oral anticoagulants, sulfonylureas, phenytoin. American Academy of Pediatrics expresses concern about breast- feeding while taking benzodiazepines. Contraindications: Hypersensitivity to benzodiazepines, preg- nancy, narrow-angle glaucoma. These effects result in increased force of cardiac muscle contraction and vasodilation. Adjustment of dosage • Kidney disease: Creatinine clearance <50 mL/min: reduce infusion rate of milrinone; creatinine clearance 50 mL/min per 1. Warnings/precautions: Use with caution in patients with ventric- ular arrhythmias, atrial fibrillation or flutter, obstructive disorders of the aortic or pulmonic valve, renal impairment, electrolyte abnormalities. Parameters to monitor • Renal function, fluid and electrolytes, especially potassium carefully during therapy. Hence, care should be taken to monitor patients carefully during and shortly after infusion. Mechanism of action: Inhibits bacterial protein synthesis after specific ribosomal binding. Susceptible organisms in vivo: Borrelia burgdorferi, Borrelia recurrentis, Brucella sp, Calymmatobacterium granulomatis, Chla- mydia pneumoniae, Chlamydia psittaci, Chlamydia trachomatis, Ehrlichia sp, Helicobacter pylori, Q fever, Rickettsia sp, Vibrio sp. Contraindications: Hypersensitivity to any tetracycline, patients with esophageal obstruction, children <8 years. Adjustment of dosage • Kidney disease: Reduce dose by one-third usual in renal failure. Onset of Action Peak Effect Duration 30 min 2–3 h 2–5 d Food: May be taken with or without food.

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Formulations of Semisolid Drugs 141 Clotrimazole and Clindamycin Cream Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 20 buy sucralfate 1000mg mastercard gastritis symptoms nausea. Add into step 2 with vigorous mixing to form 100 mg clotrimazole and 20 mg clindamycin buy sucralfate 1000 mg free shipping gastritis diet 1234. Clotrimazole and Clindamycin Suppositories Bill of Materials Scale (mg/suppository) Item Material Name Quantity/1000 Suppositories (g) 100 sucralfate 1000mg cheap gastritis diet . Coal Tar and Allantoin Cream Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 40 buy sucralfate 1000 mg on line gastritis bile reflux diet. Slowly add water phase in increments to the oil ther homogenization may improve stability phase. Formulations of Semisolid Drugs 143 Coal Tar and Allantoin Cream Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 160. Inactive ingre- methylchloroisothiazolinone, methylisothiazolinone, min- dients include acetylated lanolin alcohol, alcohol (4. Collagenase Ointment Collagenase ointment is a sterile enzymatic debriding from the fermentation by Clostridium histolyticum. Conjugated Estrogens Vaginal Cream Each gram of conjugated estrogens vaginal cream contains exclusively from natural sources, occurring as the sodium 0. It contains estrone, equilin, and 17 (alpha)- methyl stearate, benzyl alcohol, sodium lauryl sulfate, dihydroequilin, together with smaller amounts of 17 glycerin, and mineral oil. Cyanocobalamin gel for intranasal administration is equivalent vitamin B12 activity. It is solution of cyanocobalamin with methylcellulose, sodium very hygroscopic in the anhydrous form and sparingly to citrate, citric acid, glycerin, and benzalkonium chloride in moderately soluble in water (1:80). After initial priming, each metered gel delivers an oxidizing or reducing agents (vitamin C), but not by auto- average of 500 mcg of cyanocobalamin, and the 2. Prepare a dispersion of item 1 in balance of item 3 in a separate vessel and add to step 2. Each gram of synthetic nonfluorinated corticosteroid, for topical derma- lotion contains 0. The corticosteroids constitute a class of pri- lauryl sulfate, light mineral oil, cetyl alcohol, stearyl alco- marily synthetic steroids used topically as anti-inflamma- hol, propylene glycol, methylparaben, propylparaben, sor- tory and antipruritic agents. Dexamethasone Sodium Phosphate Ointment Dexamethasone sodium phosphate is 9-fluoro-11(beta), topical steroid ointment containing dexamethasone sodium 17-dihydroxy-16(alpha)-methyl-21-(phosphonooxy)pre- phosphate equivalent to 0. Inactive ingredients are white thalmic ointment dexamethasone sodium phosphate is a petrolatum and mineral oil. Dexpanthenol Cream Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 5. Add items 11 and 12 and mix (without vacuum) and item 9 and heat to 70°C and mix for 10 and cool down to 25°C. In a separate container add and dissolve items 7 and 8 in item 6 at 70°C and add to step 2. Cool to room temperature, stirring continuously water, add liquid paraffin, and stir, heating to until the air bubbles disappear. Diclofenac Diethylamine Gel Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 1. Charge 90% of item 11 in a mixing vessel, heat and then add to step 5 and mix for 10 minutes, to 80°C; stir to produce vortex and add item 2 7. Dissolve item 1 in items 3 and 4 separately and to disperse after passing through 1-mm sieve; transfer to step 6 through a cloth filter; mix for mix for 5 minutes, avoiding foam. Formulations of Semisolid Drugs 147 Diclofenac Diethylammonium Gel Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) q. Place water purified and alcohol in a 316 grade carbomer swells completely in the hydroalco- stainless steel mixing tank. Diclofenac Sodium Suppositories Bill of Materials Scale (mg/suppository) Item Material Name Quantity/1000 Suppositories (g) 12. Diclofenac Sodium Suppositories Bill of Materials Scale (mg/suppository) Item Material Name Quantity/1000 Suppositories (g) 50. Formulations of Semisolid Drugs 149 Diclofenac Sodium Suppositories Bill of Materials Scale (mg/suppository) Item Material Name Quantity/1000 Suppositories (g) 100. Dichlorobenzyl Alcohol Tooth Gel Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 1. Dienestrol Vaginal Cream The active ingredient in dienestrol vaginal cream is dienes- acid, butylated hydroxyanisole, citric acid, sodium trol 0. Transfer molten fat at 70°C after passing vessel at 79°–75°C; hold molten fat at 70°C through a stainless steel filter to step above with continuous stirring at low speed. Homogenize at slow speed for 10 minutes; tem- add and dissolve parabens by stirring. In a separate vessel, take the balance of item 5 salicylate solution to the cream at 50°C while and sodium hydroxide pellets and sodium phos- stirring. Transfer step 3 to the paraben solution and mix for lavender oil, and glycerin at 40°C. Each diacetate in an emollient, occlusive base consisting of gram of cream contains 0. Inactive ingre- light mineral oil, ozokerite, paraffin, propylene glycol, dients include aloe extract, benzyl alcohol, cod liver oil sorbitol, synthetic beeswax, and water. Dinoprostone Cervical Gel Dinoprostone is the naturally occurring form of prostaglan- ular weight is 352. Dinoprostone Vaginal Insert and Suppositories Dinoprostone vaginal insert is a thin, flat, polymeric slab of 65°–69°C. Dinoprostone is soluble in ethanol and in that is rectangular with rounded corners, contained within 25% ethanol in water. Each insert contains 10 mg of the pouch of a knitted polyester retrieval system, an inte- dinoprostone in 241 mg of a cross-linked polyethylene gral part of which is a long tape. Each slab is buff colored oxide/urethane polymer that is a semiopaque, beige-col- and semitransparent and contains 10 mg of dinoprostone. The insert and its retrieval sys- off-white knitted polyester retrieval system designed to tem, made of polyester yarn, are nontoxic, and when aid retrieval at the end of the dosing interval. The finished placed in a moist environment, they absorb water, swell, product is a controlled release formulation that has been and release dinoprostone. The insert contains 10 mg dino- found to release dinoprostone in vivo at a rate of approx- prostone. Each 11(alpha),15S-dihydroxy-9-oxo-prosta-5Z,13E-dien-1- suppository contains 20 mg of dinoprostone in a mixture oic acid. It has a melting point within the range Diphenhydramine Hydrochloride and Zinc Acetate Ointment Diphenhydramine hydrochloride and zinc acetate oint- 0. Inactive ingredients include cetyl alcohol, diazolid- ment contain diphenhydramine hydrochloride 1% and inyl urea, methylparaben, polyethylene glycol monostear- zinc acetate 0. The extra-strength formulation is ate 1000, propylene glycol, propylparaben, and purified diphenhydramine hydrochloride 2% and zinc acetate water. Inac- propylene glycol, purified water, sucrose distearate, and tive ingredients include benzyl alcohol, light mineral oil, sucrose stearate. Econazole Nitrate and Benzoyl Peroxide Lotion Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 50. Other thine hydrochloride as eflornithine hydrochloride mono- ingredients include ceteareth-20, cetearyl alcohol, dime- hydrate (150 mg/g). Formulations of Semisolid Drugs 153 Enzyme Extract Ointment Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 50. Erythromycin Ointment Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 10. Run through 200 mesh (74-µm aperture) screen on Homoloid mill directly into main portion of 1. Erythromycin and Neomycin Ointment Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 10.

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